Open AccessIndomethacin Suppresses the Growth of Colon 26, Meth‐A and FM3A Tumors in Mice by Reducing the Prostaglandin E 2 Content and Telomerase Activity in Tumor Tissues
Author(s) -
Ogino Mitsuharu,
Hisatomi Hisashi,
Murata Minoru,
Hanazono Makoto
Publication year - 1999
Publication title -
japanese journal of cancer research
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 2.035
H-Index - 141
eISSN - 1349-7006
pISSN - 0910-5050
DOI - 10.1111/j.1349-7006.1999.tb00812.x
Subject(s) - telomerase , meth , prostaglandin e2 , in vivo , prostaglandin , spleen , medicine , somatic cell , endocrinology , chemistry , biology , biochemistry , microbiology and biotechnology , monomer , organic chemistry , acrylate , gene , polymer
The antitumor effect of indomethacin on Colon 26, Meth‐A and FM3A tumors was investigated in mice. The prostaglandin E 2 content in tumor tissues was assayed to find out if indomethacin acts on tumors, and the telomerase activity in tumors and somatic tissues (testis, liver, spleen and colon) was also monitored during indomethacin treatment. Growth of Colon 26, Meth‐A and FM3A tumors was significantly ( P < 0.001‐0.05) suppressed by indomethacin compared to the untreated controls. The prostaglandin E2 content in the three tumors was markedly ( P < 0.001) reduced by indomethacin. Telomerase activity in Colon 26 and FM3A tumors was significantly ( P < 0.001) lower than that of untreated tumors (80% and 45% decrease versus the controls, respectively), and the activity in Meth‐A tumor was slightly decreased (10% decrease versus the control) by indomethacin. Telomerase activity in the somatic tissues was not significantly affected by indomethacin. In summary, this study shows the effectiveness of indomethacin as an antitumor agent against three types of tumors, and suggests that indomethacin affects telomerase activity in tumors in vivo.